Background: Hypersensitivity reactions to benzodiazepines, although uncommon, represent a clinically relevant issue in perioperative practice. Benzodiazepines are widely used medications with anxiolytic, sedative, and anticonvulsant properties. The objective of this review is to synthesize current knowledge on benzodiazepine hypersensitivity, focusing on underlying mechanisms, clinical manifestations, diagnostic considerations, and strategies for management and prevention in the perioperative setting. Methodology: A narrative synthesis of the current literature on hypersensitivity reactions to benzodiazepines was performed. The review included published case reports, case series, and clinical studies describing hypersensitivity reactions, their clinical presentation, and diagnostic approaches. Particular attention was given to both immunological and non-immunological mechanisms, reported clinical phenotypes, and issues relevant to perioperative patient safety. Results: The extant evidence suggests that benzodiazepine hypersensitivity may involve both immunological and non-immunological pathways. The spectrum of reported reactions encompasses mild cutaneous manifestations and severe systemic responses, although the incidence remains low. This review highlights diagnostic challenges related to variable clinical presentation and the limited availability of standardized testing methods. Conclusions: Although cases of benzodiazepine hypersensitivity are uncommon, awareness of potential reactions is critical for ensuring safe clinical practice. This review emphasizes the necessity for additional research to elucidate the underlying mechanisms, standardize the diagnostic criteria, and formulate management protocols.

The conceptualization of Parkinson’s disease (PD) has shifted from a strictly central neurodegenerative disorder to a systemic synucleinopathy that may, in some patients, originate in the enteric nervous system. This review synthesizes recent evidence highlighting the potential role of sulfate-reducing Desulfovibrio (DSV) bacteria as candidate pathobionts in the proposed “gut-first” pathogenic cascade. By colonizing anaerobic niches within the colon and metabolizing dietary sulfur compounds, DSV generate hydrogen sulfide (H₂S), a gaseous metabolite that may compromise intestinal barrier integrity and impair mitochondrial function through the inhibition of cytochrome c oxidase. These processes have been associated with ATP depletion, cytochrome c release, and iron-dependent oxidative stress, creating conditions that may favor α-synuclein misfolding and aggregation within enteroendocrine cells. We further examine evidence supporting the retrograde propagation of α-synuclein pathology from the gut to the brain via the vagus nerve—a hypothesis strengthened by experimental findings and epidemiological observations, including studies reporting reduced PD risk following truncal vagotomy. Although the increased prevalence of DSV in PD patients suggests potential applications in prodromal diagnostics and microbiome-based risk stratification, a definitive causal relationship has yet to be established. We therefore discuss key methodological limitations, including biases associated with 16S rRNA sequencing and the current lack of robust in vivo metabolomic evidence. Finally, we consider whether targeted modulation of the intestinal environment, including DSV-specific bacteriophages and [FeFe]-hydrogenase inhibitors, could emerge as a future strategy for influencing early disease processes.